Doseff A I, Arndt K T
Cold Spring Harbor Laboratory, New York 11724-2212, USA.
Genetics. 1995 Nov;141(3):857-71. doi: 10.1093/genetics/141.3.857.
Saccharomyces cerevisiae mutations that cause a requirement for SSD1-v for viability were isolated, yielding one new gene, LAS1, and three previously identified genes, SIT4, BCK1/SLK1, and SMP3. Three of these genes, LAS1, SIT4, and BCK1/SLK1, encode proteins that have roles in bud formation or morphogenesis. LAS1 is essential and loss of LAS1 function causes the cells to arrest as 80% unbudded cells and 20% large budded cells that accumulate many vesicles at the mother-daughter neck. Overexpression of LAS1 results in extra cell surface projections in the mother cell, alterations in actin and SPA2 localization, and the accumulation of electron-dense structures along the periphery of both the mother cell and the bud. The nuclear localization of LAS1 suggests a role of LAS1 for regulating bud formation and morphogenesis via the expression of components that function directly in these processes.
分离出了酿酒酵母中导致对SSD1-v有生存能力需求的突变,得到一个新基因LAS1,以及三个先前已鉴定的基因SIT4、BCK1/SLK1和SMP3。其中三个基因LAS1、SIT4和BCK1/SLK1编码在芽形成或形态发生中起作用的蛋白质。LAS1是必需的,LAS1功能丧失会导致细胞停滞,80%为未出芽细胞,20%为大芽细胞,这些细胞在母-子颈部积累许多囊泡。LAS1的过表达导致母细胞出现额外的细胞表面突起、肌动蛋白和SPA2定位改变,以及母细胞和芽的周边积累电子致密结构。LAS1的核定位表明LAS1通过直接在这些过程中起作用的成分的表达来调节芽形成和形态发生。